Tag Archives: TBI

Day three is Air Ambulance and pre-hospital day and the great and the good are here en mass.
The heavy weights are coming out to make their points…..

Unarguably the best lecture of the day was delivered by our very own Cliff Reid on prehospital training. Using Sydney HEMS induction training he highlighted the challenges posed to prehospital services training doctors and paramedics rotating through the service.

Turning a good inhospital doctor into a great prehospital one in the space of an induction program requires focus. Knowledge is therefore not the focus of training, performance is. Often doctors already possess the clinical skills and knowledge and it is the application of these pre existing skills in challenging environments when cognitively overloaded that is the key.

The Sydney HEMS program provides the mindware and communication skills the practitioner needs to do this and drills these skills in simulated environments. He uses perturbation, so like the Bruce protocol exercise test the simulations just get harder until you are at the very limits of your bandwidth. Debriefing of course is important but the recommended protracted debrief is often impractical and unnecessary so simulations designed with cognitive traps are used to highlight learning points and are drilled until the message is received. In this way tress exposure enhances cognitive resilience. And importantly they use cross training, so the doctors and the paramedics undergo the same program so each member of the team understands the challenges faced by the other.

Does this sound like fun? For the shrinking violets out there it could be seen as threatening. But for the adrenaline junkies…….hell yeah!

It’s truly a training ethos that I buy into and I’d love to be able to achieve that standard of training in my own service.

How would you transfer a psychotic patient requiring specialist intervention that can only be received after aeromedical transfer? Stefan Mazur of MedSTAR, the retrieval service in South Australia shared their experience with ketamine to facilitate the safe transfer of these patients with no reports of adverse effects on the mental state of the patient, as first described by Minh Le Cong and colleagues. Is there no end to the usefulness of this drug? No wonder we’re experiencing a supply issue in the UK!

And finally, the ultimate reflective practice should include the post mortem of our critically sick patients. The approach the forensic pathologist takes is similar to a clinician (with the time pressure removed). They read the scene and use this information to predict injuries (sound familiar?). Post mortem CT scanning with recon provides yet another layer of information. We are missing a trick if we don’t seek this feedback to correlate with our clinical findings. Even better, rare practical skills are often routinely performed as part of the post mortem – we should be making use of this opportunity to train.

Almost two-thirds of patients with extradural haematoma and bilateral fixed dilated pupils survived after surgery, with over half having a good outcome

Neurosurgeon, HEMS doctor, and all round good egg Mark Wilson was on the RAGE podcast recently and mentioned favourable outcomes from neurosurgery in patients with extradural (=epidural) haematomas who present with bilateral fixed dilated pupils (BFDP). Here’s his paper that gives the figures – a systematic review and meta-analysis.

A total of 82 patients with BFDP who underwent surgical evacuation of either subdural or extradural haematoma were identified from five studies – 57 with subdural (SDH) and 25 with extradural haematomas (EDH).

In patients with EDH and BFDP mortality was 29.7% (95% CI 14.7% to 47.2%) and 54.3% had a favourable outcome (95% CI 36.3% to 71.8%).

Only 6.6% of patients with SDH and BFDP had a good functional outcome.

Clearly there is potential for selection bias and publication bias, but these data certainly suggest an aggressive surgical approach is appropriate in some patients with BFDP.

The authors comment on the pessimism that accompanies these cases, which potentially denies patients opportunities for recovery:

“We believe that 54% of patients with extradural haematoma with BFDPs having a good outcome is an underappreciated prognosis, and the perceived poor prognosis of BFDPs (from all causes) has influenced decision making deeming surgery inappropriately futile in some cases.”

Primary objective To review the prognosis of patients with bilateral fixed and dilated pupils secondary to traumatic extradural (epidural) or subdural haematoma who undergo surgery.

Methods A systematic review and meta-analysis was performed using random effects models. The Cochrane Central Register of Controlled Trials and PubMed databases were searched to identify relevant publications. Eligible studies were publications that featured patients with bilateral fixed and dilated pupils who underwent surgical evacuation of traumatic extra-axial haematoma, and reported on the rate of favourable outcome (Glasgow Outcome Score 4 or 5).

Results Five cohort studies met the inclusion criteria, collectively reporting the outcome of 82 patients. In patients with extradural haematoma, the mortality rate was 29.7% (95% CI 14.7% to 47.2%) with a favourable outcome seen in 54.3% (95% CI 36.3% to 71.8%). In patients with acute subdural haematoma, the mortality rate was 66.4% (95% CI 50.5% to 81.9%) with a favourable outcome seen in 6.6% (95% CI 1.8% to 14.1%).

Conclusions and implications of key findings Despite the poor overall prognosis of patients with closed head injury and bilateral fixed and dilated pupils, our findings suggest that a good recovery is possible if an aggressive surgical approach is taken in selected cases, particularly those with extradural haematoma.

It’s the last day of the conference and new this year is the Neurotrauma Masterclass running in parallel with the main track which focuses on in-hospital care.

We heard a little from Mark Wilson yesterday. He believes we are missing a pre-hospital trick in traumatic brain injury. Early intervention is the key (he has data showing aggressive intervention for extradural haemorrhage in patients with fixed dilated pupils has good outcomes in 75%).

Today he taught us neurosurgery over lunch. If you have a spare moment over then go to his website and you too can learn how to be a brain surgeon!

Dr Gareth Davies talks about Impact Brain Apnoea. Many will not heard of this phenomenon. Clinicians rarely see patients early enough in their injury timeline to witness

Essentially this term describes the cessation of breathing after head injury. It has been described in older texts (first mentioned in 1894!) The period of apnoea increases with the severity of the injury and if non fatal will then recover to normal over a period of time. Prolonged apnoea results in hypotension.

This is a brain stem mediated effect with no structural injury.

The effect is exacerbated by alcohol and ameliorated by ventilatory support during the apnoeic phase.

Associated with this response is a catecholamine surge which exacerbates the cardiovascular collapse and he introduces the concept of Central Shock.

So how does this translate into the real world?

Well, could we be miscategorising patients that die before they reach hospital as succumbing to hypovolaemic when in fact they had central shock?

These patients essentially present with respiratory arrest, but do well with supported ventilation. Identification of these patients by emergency dispatchers with airway support could mean the difference between life and death.

Prof Monty Mythen spoke on fluid management in the trauma patient after blood (not albumin, HES or colloids) and Prof Mervyn Singer explained the genetic contribution to the development of MODS after trauma.

Prof Brohi gave us the lowdown on trauma laparotomies – not all are the same! With important human factors advice:

Prof Susan Brundage is a US trauma surgeon who has been recruited into the Bart’s and the London School of Medicine and the Royal College of Surgeons of England International Masters in Trauma Sciences for her trauma expertise.

She tells us that MOOCs and FOAM are changing education. Whilst education communities are being formed, she warns of the potential pitfalls of this form of education with a proportion of participants not fully engaged.

The Masters program is growing and if you’re interested you can read more here.

Objective Various intracranial pathologies in traumatic brain injury (TBI) can help to predict patient outcomes.
These pathologies can be categorised using the Marshall Classiﬁcation or the Abbreviated Injury Scale (AIS) dictionary or can be described through traditional descriptive terms such as subarachnoid haemorrhage (SAH), subdural haemorrhage (SDH), epidural haemorrhage (EDH) etc. The purpose of this study is to assess the prognostic value of AIS scores, the Marshall Classiﬁcation and various intracranial pathologies in TBI.

Methods A dataset of 802 TBI patients in the Trauma Audit and Research Network (TARN) database was analysed using logistic regression. First, a baseline model was constructed with age, Glasgow Coma Scale (GCS), pupillary reactivity, cause of injury and presence/absence of extracranial injury as predictors and survival at discharge as the outcome. Subsequently, AIS score, the Marshall Classiﬁcation and various intracranial pathologies such as haemorrhage, SAH or brain swelling were added in order to assess the relative predictive strength of each variable and also to assess the improvement in the performance of the model.

Results Various AIS scores or Marshal classes did not appear to signiﬁcantly affect the outcome. Among traditional descriptive terms, only brain stem injury and brain swelling signiﬁcantly inﬂuenced outcome [odds ratios for survival: 0.17 (95% conﬁdence interval [CI]; 0.08–0.40) and 0.48 (95% CI; 0.29–0.80), respectively].
Neither haemorrhage nor its subtypes, such as SAH, SDH and EDH, were signiﬁcantly associated with outcome. Adding AIS scores, the Marshall Classiﬁcation and various
intracranial pathologies to the prognostic models resulted in an almost equal increase in the predictive performance of the baseline model.

Conclusions In this relatively recent dataset, each of the brain injury classification systems enhanced equally the performance of an early mortality prediction model in traumatic brain injury patients. The significant effect of brain swelling and brain stem injury on the outcome in comparison to injuries such as SAH suggests the need to improve therapeutic approaches to patients who have sustained these injuries.

A South American randomised controlled trial has demonstrated no improvement in mortality when traumatic brain injured patients had therapy targeted at keeping intracranial pressure below or equal to 20 mmHg as measured by an intraparenchymal monitor. The control group’s management was guided by neurologic examination and serial CT imaging(1).

Editorialist Dr Ropper summarises what we should do with this information well(2):

“[The authors]…do not advocate abandoning the treatment of elevated intracranial pressure any more than the authors of studies on wedge pressure reject the administration of fluid boluses in the treatment of shock”

BACKGROUND

Intracranial-pressure monitoring is considered the standard of care for severe traumatic brain injury and is used frequently, but the efficacy of treatment based on monitoring in improving the outcome has not been rigorously assessed.

METHODS
We conducted a multicenter, controlled trial in which 324 patients 13 years of age or older who had severe traumatic brain injury and were being treated in intensive care units (ICUs) in Bolivia or Ecuador were randomly assigned to one of two specific protocols: guidelines-based management in which a protocol for monitoring intraparenchymal intracranial pressure was used (pressure-monitoring group) or a protocol in which treatment was based on imaging and clinical examination (imaging–clinical examination group). The primary outcome was a composite of survival time, impaired consciousness, and functional status at 3 months and 6 months and neuropsychological status at 6 months; neuropsychological status was assessed by an examiner who was unaware of protocol assignment. This composite measure was based on performance across 21 measures of functional and cognitive status and calculated as a percentile (with 0 indicating the worst performance, and 100 the best performance).

RESULTS
There was no significant between-group difference in the primary outcome, a composite measure based on percentile performance across 21 measures of functional and cognitive status (score, 56 in the pressure-monitoring group vs. 53 in the imaging–clinical examination group; P=0.49). Six-month mortality was 39% in the pressure-monitoring group and 41% in the imaging–clinical examination group (P=0.60). The median length of stay in the ICU was similar in the two groups (12 days in the pressure-monitoring group and 9 days in the imaging–clinical examination group; P=0.25), although the number of days of brain-specific treatments (e.g., administration of hyperosmolar fluids and the use of hyperventilation) in the ICU was higher in the imaging–clinical examination group than in the pressure-monitoring group (4.8 vs. 3.4, P=0.002). The distribution of serious adverse events was similar in the two groups.

CONCLUSIONS
For patients with severe traumatic brain injury, care focused on maintaining monitored intracranial pressure at 20 mm Hg or less was not shown to be superior to care based on imaging and clinical examination

Full text access is only available to New England Journal subscribers, but I’ve summarised some of the interesting bits in a short quiz you can take to test your knowledge. Just 13 True/False questions.

Two papers examining the same massive European trauma dataset identify risk factors for spinal injury. The first examined all spinal injury(1), and the most recent focuses on cervical injury(2). Male gender, decreased GCS, falls > 2m, sports injuries, and road traffic collisions were predictors of any fracture/dislocation or cord injury. Head injury was not an independent risk factor, contrary to much popular teaching. I’ve summarised the two papers’ findings in this table. The odds ratios are reported in the abstracts.

Patients with cervical spine injuries are a high-risk group, with the highest reported early mortality rate in spinal trauma.

METHODS: This cohort study investigated predictors for cervical spine injury in adult (≥ 16 years) major trauma patients using prospectively collected data of the Trauma Audit and Research Network from 1988 to 2009. Univariate and multivariate logistic regression analyses were used to determine predictors for cervical fractures/dislocations or cord injury.

Threshold for treatment of intracranial hypertension
Treatment of intracranial pressure (ICP) may be considered at a threshold of 20 mm Hg (Grade C).

Sustained elevations in ICP (>20 mm Hg) are associated with poor outcome in children after severe TBI. Normal values of blood pressure and ICP are age-dependent (lower at younger ages), so it is anticipated that the optimal ICP treatment threshold may be age-dependent.

Cerebral perfusion pressure thresholds
A CPP threshold 40–50 mm Hg may be considered. There may be age-specific thresholds with infants at the lower end and adolescents at the upper end of this range (Grade C).

CPP should be determined in a standard fashion with ICP zeroed to the tragus (as an indicator of the foramen of Monro and midventricular level) and MAP zeroed to the right atrium with the head of the bed elevated 30°.

Neuroimaging
In the absence of neurologic deterioration or increasing intracranial pressure (ICP), obtaining a routine repeat computed tomography (CT) scan >24 hrs after the admission and initial follow-up study may not be indicated for decisions about neurosurgical intervention (Grade C).

Hyperosmolar therapy
Hypertonic saline should be considered for the treatment of severe pediatric traumatic brain injury (TBI) associated with intracranial hypertension. Effective doses for acute use range between 6.5 and 10 mL/kg (of 3%) (Grade B).

Hypertonic saline should be considered for the treatment of severe pediatric TBI associated with intracranial hypertension. Effective doses as a continuous infusion of 3% saline range between 0.1 and 1.0 mL/kg of body weight per hour administered on a sliding scale. The minimum dose needed to maintain intracranial pressure (ICP)

Temperature control
Moderate hypothermia (32–33°C) beginning early after severe traumatic brain injury (TBI) for only 24 hrs’ duration should be avoided.
Moderate hypothermia (32–33°C) be- ginning within 8 hrs after severe TBI for up to 48 hrs’ duration should be considered to reduce intracranial hypertension.
If hypothermia is induced for any indication, rewarming at a rate of >0.5°C/hr should be avoided (Grade B).

Moderate hypothermia (32–33°C) be- ginning early after severe TBI for 48 hrs, duration may be considered (Grade C).Note: after completion of these guidelines, the committee became aware that the Cool Kids trial of hypothermia in pediatric TBI was stopped because of futility. The implications of this development on the recommendations in this section may need to be considered by the treating physician when details of the study are published.

Cerebrospinal fluid drainage
Cerebrospinal fluid (CSF) drainage through an external ventricular drain may be considered in the management of increased intracranial pressure (ICP) in children with severe traumatic brain injury (TBI).
The addition of a lumbar drain may be considered in the case of refractory intracranial hypertension with a functioning external ventricular drain, open basal cis- terns, and no evidence of a mass lesion or shift on imaging studies (Grade C).

Decompressive craniectomy for the treatment of intracranial hypertension
Decompressive craniectomy (DC) with duraplasty, leaving the bone flap out, may be considered for pediatric patients with traumatic brain injury (TBI) who are showing early signs of neurologic deterioration or herniation or are developing intracranial hypertension refractory to medical management during the early stages of their treatment (Grade C).

Hyperventilation
Avoidance of prophylactic severe hyperventilation to a PaCO2 If hyperventilation is used in the management of refractory intracranial hypertension, advanced neuromonitoring for evaluation of cerebral ischemia may be considered (Grade C).

Corticosteroids
The use of corticosteroids is not recommended to improve outcome or reduce intracranial pressure (ICP) for children with severe traumatic brain injury (TBI) (Grade B).

Analgesics, sedatives, and neuromuscular blockade
Etomidate may be considered to control severe intracranial hypertension; however, the risks resulting from adrenal suppression must be considered.
Thiopental may be considered to control intracranial hypertension.
In the absence of outcome data, the specific indications, choice and dosing of analgesics, sedatives, and neuromuscular-blocking agents used in the management of infants and children with severe traumatic brain injury (TBI) should be left to the treating physician.
*As stated by the Food and Drug Administration, continuous infusion of propofol for either sedation or the management of refractory intracranial hypertension in infants and children with severe TBI is not recommended (Grade C).

The availability of other sedatives and analgesics that do not suppress adrenal function, small sample size and single-dose administration in the study discussed previously, and limited safety profile in pediatric TBI limit the ability to endorse the general use of etomidate as a sedative other than as an option for single-dose administration in the setting of raised ICP.

Glucose and nutrition
The evidence does not support the use of an immune-modulating diet for the treatment of severe traumatic brain injury (TBI) to improve outcome (Grade B).

In the absence of outcome data, the specific approach to glycemic control in the management of infants and children with severe TBI should be left to the treating physician (Grade C).

Antiseizure prophylaxis
Prophylactic treatment with phenytoin may be considered to reduce the incidence of early posttraumatic seizures (PTS) in pediatric patients with severe traumatic brain injury (TBI) (Grade C).

The incidence of early PTS in pediatric patients with TBI is approximately 10% given the limitations of the available data. Based on a single class III study (4), prophylactic anticonvulsant therapy with phenytoin may be considered to reduce the incidence of early posttraumatic seizures in pediatric patients with severe TBI. Concomitant monitoring of drug levels is appropriate given the potential alterations in drug metabolism described in the context of TBI. Stronger class II evidence is available supporting the use of prophylactic anticonvulsant treatment to reduce the risk of early PTS in adults. There are no compelling data in the pediatric TBI literature to show that such treatment reduces the long-term risk of PTS or improves long-term neurologic outcome.

Just in case you thought you might be missing some recent gem on what we should be giving patients with traumatic brain injury in the field: a team from Melbourne has reviewed the literature and concluded isotonic crystalloids (Ringer’s or Saline) are as good as anything else.

The early management of patients who have sustained traumatic brain injury is aimed at preventing secondary brain injury through avoidance of cerebral hypoxia and hypoperfusion. Especially in hypotensive patients, it has been postulated that hypertonic crystalloids and colloids might support mean arterial pressure more effectively by expanding intravascular volume without causing problematic cerebral oedema. We conducted a systematic review to investigate if hypertonic saline or colloids result in better outcomes than isotonic crystalloid solutions, as well as to determine the safety of minimal volume resuscitation, or delayed versus immediate fluid resuscitation during prehospital care for patients with traumatic brain injury. We identified nine randomized controlled trials and one cohort study examined the effects of hypertonic solutions (with or without colloid added) for prehospital fluid resuscitation. None has reported better survival and functional outcomes over the use of isotonic crystalloids. The only trial of restrictive resuscitation strategies was underpowered to demonstrate its safety compared with aggressive early fluid resuscitation in head injured patients, and maintenance of cerebral perfusion remains the top priority.

What are the best sedatives for patients with traumatic brain injury? A systematic review found no evidence that one sedative agent is better than another for improvement of neurologic outcome or mortality in critically ill adults with severe TBI. Thirteen randomised trials including around 380 patients were reviewed.

Why sedate brain injured patients anyway? Reasons include:

minimise noxious stimuli

improve patient comfort

reduce metabolic requirements of the injured brain to avoid ischemic progression of the traumatic lesion in presence of increased ICP

facilitate mechanical ventilation to control PaCo2

avoid ICP rises due to airway instrumentation such as those induced by coughing

Interestingly boluses or short infusions of opioids resulted in (often transient) increases in ICP and decreases in MAP and CPP in three RCTs. An accompanying editorial suggests this may be due to large opioid doses (up to 3 μg/kg of fentanyl) and consequent hypotension; hypotension itself may trigger autoregulatory cerebral vasodilatation and increase ICP and decrease CPP. Although opioids have been linked with increased ICP through decreased cerebrovascular resistance, increased cerebral blood flow or Paco2, and disturbed cerebral autoregulation, they state that in studies in which hypotension after opioid administration was prevented, an ICP increasing effect was not seen. It is important to note the small sample sizes studied and the long time period of studies included, dating back some decades.

Importantly, ketamine did not result in the increase in ICP purported by older literature.

DATA EXTRACTION: In duplicate and independently, two investigators extracted data and evaluated methodologic quality and results.

DATA SYNTHESIS: Among 1,892 citations, 13 randomized controlled trials enrolling 380 patients met inclusion criteria. Long-term sedation (≥24 hrs) was addressed in six studies, whereas a bolus dose, short infusion, or doubling of plasma drug concentration was investigated in remaining trials. Most trials did not describe baseline traumatic brain injury prognostic factors or important cointerventions. Eight trials possibly or definitely concealed allocation and six were blinded. Insufficient data exist regarding the effects of sedative agents on neurologic outcome or mortality. Although their effects are likely transient, bolus doses of opioids may increase intracranial pressure and decrease cerebral perfusion pressure. In one study, a long-term infusion of propofol vs. morphine was associated with a reduced requirement for intracranial pressure-lowering cointerventions and a lower intracranial pressure on the third day. Trials of propofol vs. midazolam and ketamine vs. sufentanil found no difference between agents in intracranial pressure and cerebral perfusion pressure.

CONCLUSIONS: This systematic review found no convincing evidence that one sedative agent is more efficacious than another for improvement of patient-centered outcomes, intracranial pressure, or cerebral perfusion pressure in critically ill adults with severe traumatic brain injury. High bolus doses of opioids, however, have potentially deleterious effects on intracranial pressure and cerebral perfusion pressure. Adequately powered, high-quality, randomized controlled trials are urgently warranted.